The majority of prostate cancers detected through PSA screening harbor an acquired recurrent chromosomal rearrangement (Tomlins et al., Science, 310, 644-8, 2005). The promoter region of the androgen-regulated transmembrane protease, serine 2 (TMPRSS2) gene is most often fused to the coding region of members of the erythroblast transformation specific (ETS) family of transcription factors, most commonly v-ets erythroblastosis virus E26 oncogene homolog (avian) (ERG). The TMPRSS2-ERG fusion is observed in around 90% of tumors that over-express the oncogene ERG. Other, less common, fusion events occur involving ETS family members (ETV1, ETV4 and ETV5) fused to TMPRSS2 or other 5′ partners that differ in their prostate specificity and response to androgen (SLC45A3, HERV-K, C15orf21, HNRPA2B1, FLJ35294, DDX5, CANT1 and KLK2, reviewed by Kumar-Sinha et al., Nat Rev Cancer 8(7):497-511, 2008; and more recently, ACSL3 (Attard et al., Br J Cancer, 99, 314-20, 2008)). Moreover, variations in the structure of the gene fusions in prostate cancer yielding different fusion transcript isoforms have been reported (Wang et al., Cancer Res, 66, 8347-51, 2006). ETS rearranged prostate cancer, similar to other translocation tumors, may represent a distinct molecular subclass of prostate cancer based on studies demonstrating characteristic morphologic features (Mosquera et al., J Pathol 212: 91-1012007), natural history (Attard et al., Oncogene 27: 253-63, 2008; Demichelis et al., Oncogene 26: 4596-9, 2007) and specific genomic (Demichelis et al., Genes Chromosomes Cancer 48: 366-380, 2009) and expression profiles (Setlur et al., J Natl Cancer Inst 100: 815-25, 2008).